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Sensory findings after stimulation of the thoracolumbar fascia with hypertonic saline suggest its contribution to low back pain

Schilder, Andreasa,*; Hoheisel, Ulricha; Magerl, Waltera; Benrath, Justusb; Klein, Thomasa,c; Treede, Rolf-Detlefa

doi: 10.1016/j.pain.2013.09.025
Research papers
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Summary The human thoracolumbar fascia is more sensitive to chemical stimulations than the adjacent muscle and subcutis according to pain intensity, duration, radiation and affective descriptors.

ABSTRACT Injection of hypertonic saline into deep tissues of the back (subcutis, muscle, or the surrounding fascia) can induce acute low back pain (LBP). So far, no study has analyzed differences in temporal, qualitative, and spatial pain characteristics originating from these tissues. The current study aimed to investigate the role of the thoracolumbar fascia as a potential source of LBP. In separate sessions, 12 healthy subjects received ultrasound-guided bolus injections of isotonic saline (0.9%) or hypertonic saline (5.8%) into the erector spinae muscle, the thoracolumbar fascia (posterior layer), and the overlying subcutis. Subjects were asked to rate pain intensity, duration, quality, and spatial extent. Pressure pain thresholds were determined pre and post injection. Injections of hypertonic saline into the fascia resulted in significantly larger area under the curve of pain intensity over time than injections into subcutis (P < 0.01) or muscle (P < 0.001), primarily based on longer pain durations and, to a lesser extent, on higher peak pain ratings. Pressure hyperalgesia was only induced by injection of hypertonic saline into muscle, but not fascia or subcutis. Pain radiation and pain affect evoked by fascia injection exceeded those of the muscle (P < 0.01) and the subcutis significantly (P < 0.05). Pain descriptors after fascia injection (burning, throbbing, and stinging) suggested innervation by both A- and C-fiber nociceptors. These findings show that the thoracolumbar fascia is the deep tissue of the back that is most sensitive to chemical stimulation, making it a prime candidate to contribute to nonspecific LBP but not to localized pressure hyperalgesia.

aChair of Neurophysiology, Centre for Biomedicine and Medical Technology (CBTM), Medical Faculty Mannheim, Heidelberg University, Germany

bDepartment of Anesthesiology and Intensive Care Medicine, Medical Faculty Mannheim, Heidelberg University, Germany

cMundipharma Research GmbH & Co. KG, Höhenstraβe 10, Limburg (Lahn), Germany

* Corresponding author. Address: Department of Neurophysiology, Centre for Biomedicine and Medical Technology Mannheim (CBTM), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167 Mannheim, Germany. Tel.: +49 621 383 9926; fax: +49 621 383 9921.

E-mail address:Andreas.Schilder@medma.uni-heidelberg.de

Article history:

Received 2 July 2013

Received in revised form 17 September 2013

Accepted 20 September 2013

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

© 2014 International Association for the Study of Pain
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